A Peripheral Nerve Information Transducer for Amputees: Long-Term Multichannel Recordings from Rabbit Peripheral Nerves

1986 ◽  
Vol BME-33 (2) ◽  
pp. 203-214 ◽  
Author(s):  
David J. Edell
Author(s):  
Dina V. Rusanova ◽  
Oleg L. Lakhman ◽  
Galina M. Bodienkova ◽  
Irina V. Kudaeva ◽  
Natalya G. Kuptsova

Introduction. There is a lack of knowledge of the pathophysiological mechanisms that form peripheral nerve disorders in mercury lesions of professional origin. The study aims to reveal the mechanisms underlying peripheral nerve damage in the long-term post-contact period of chronic mercury intoxication (CMI). Materials and methods. Fifty-one people had the diagnosis of a long-term period of CMI. The post-contact period was 8.5±2.6 years. The authors compared the results with a control group of 26 healthy men who had no contact with toxic substances. Stimulating electroneuromyography was performed. We studied the body systems that could contribute to the formation of disorders in the peripheral nerves. Changes in peripheral hemodynamics were studied using reovasography. The content of autoantibodies, neuron-specific enolase, serotonin, histamine, catecholamines (epinephrine, dopamine), metanephrine, and neurotrophin-3 was reviewed. The content of ceruloplasmin, secondary products of lipid peroxidation processes, reduced glutathione, the activity of superoxide dismutase and the content of nitric oxide levels were determined. Results. The study established pathogenetic structural links of peripheral nerve disorders. The autoimmune process's role was to increase the range of antibodies to the MAG protein and increase the level of antibodies to DNA. Violations of elastic-tonic properties of peripheral vessels could be associated with the functional state of motor axons. The increased content of neurotransmitters is related to the state of peripheral blood circulation; the most pronounced changes were on the legs, which could contribute to the occurrence and maintenance of vasoconstriction. The role of oxidative stress in the formation of demyelinating disorders in patients' peripheral nerves in the long-term period of CRI is possible. Conclusion. Neuroimmunological processes has an essential role in the development of peripheral nerve demyelination was shown, which consists in an increase in the content of antibodies to the MAG protein expressed on Schwann cells of peripheral nerves and in an increase in the level of antibodies to DNA involved in the formation of demyelinating changes when exposed to metallic mercury. The revealed pathological changes in the state of the peripheral blood circulation, characterized by a violation of the vessels' elastic-tonic properties, leading to demyelination of motor axons in patients in the long-term period of CMI. The increased content of neurotransmitters in the examined is of great importance in the state of peripheral circulation. Pronounced changes in blood circulation are established on the lower extremities, which may be associated with the predominance of α-adrenergic receptors in the arterial bed and may contribute to the occurrence and maintenance of vasoconstriction in the legs. The relationship between changes in indicators of oxidative stress, consisting of a decrease in the value of superoxide dismutase and reduced glutathione, and the formation of demyelinating disorders of peripheral nerves in patients in the long-term period of CMI has been proved.


2021 ◽  
Author(s):  
Alex Lassetter ◽  
Megan Corty ◽  
Romina Barria ◽  
Amy Sheehan ◽  
Sue Aicher ◽  
...  

Axons can represent the majority of the volume of a neuron and are energetically very demanding. Specialized glia ensheathe axons and are believed to support axon function and maintenance throughout life, but molecular details of glia-neuron support mechanisms remain poorly defined. Here we identify a collection of secreted and transmembrane genes that are required in glia for long-term axon survival in vivo. We show that key components of the TGFβ superfamily are required cell-autonomously in glia for peripheral nerve maintenance, although their loss does not disrupt glial morphology. We observe age-dependent neurodegeneration in the absence of glial TGFβ signaling that can be rescued by genetic blockade of Wallerian degeneration. Our data argue that glial TGFβ signaling normally acts to promote axon survival and suppress neurodegeneration.


2021 ◽  
Vol 10 (8) ◽  
pp. 1613
Author(s):  
Alessandro Crosio ◽  
Giulia Ronchi ◽  
Benedetta Elena Fornasari ◽  
Simonetta Odella ◽  
Stefania Raimondo ◽  
...  

As a consequence of trauma or surgical interventions on peripheral nerves, scar tissue can form, interfering with the capacity of the nerve to regenerate properly. Scar tissue may also lead to traction neuropathies, with functional dysfunction and pain for the patient. The search for effective antiadhesion products to prevent scar tissue formation has, therefore, become an important clinical challenge. In this review, we perform extensive research on the PubMed database, retrieving experimental papers on the prevention of peripheral nerve scarring. Different parameters have been considered and discussed, including the animal and nerve models used and the experimental methods employed to simulate and evaluate scar formation. An overview of the different types of antiadhesion devices and strategies investigated in experimental models is also provided. To successfully evaluate the efficacy of new antiscarring agents, it is necessary to have reliable animal models mimicking the complications of peripheral nerve scarring and also standard and quantitative parameters to evaluate perineural scars. So far, there are no standardized methods used in experimental research, and it is, therefore, difficult to compare the results of the different antiadhesion devices.


2018 ◽  
Vol 129 (3) ◽  
pp. 805-814 ◽  
Author(s):  
Eric D. Young ◽  
Davis Ingram ◽  
William Metcalf-Doetsch ◽  
Dilshad Khan ◽  
Ghadah Al Sannaa ◽  
...  

OBJECTIVEWhile sporadic peripheral schwannomas (SPSs) are generally well treated with surgery, their biology is not well understood. Consequently, treatment options are limited. The aim of this study was to provide a comprehensive description of SPS. The authors describe clinicopathological features and treatment outcomes of patients harboring these tumors, and they assess expression of biomarkers using a clinically annotated tissue microarray. Together, these data give new insight into the biology and management of SPS.METHODSPatients presenting with a primary SPS between 1993 and 2011 (n = 291) were selected from an institutional registry to construct a clinical database. All patients underwent follow-up, and short- and long-term outcomes were assessed. Expression of relevant biomarkers was assessed using a new tissue microarray (n = 121).RESULTSSPSs were generally large (mean 5.5 cm) and frequently painful at presentation (55%). Most patients were treated with surgery (80%), the majority of whom experienced complete resolution (52%) or improvement (18%) of their symptoms. Tumors that were completely resected (85%) did not recur. Some patients experienced short-term (16%) and long-term (4%) complications postoperatively. Schwannomas expressed higher levels of platelet-derived growth factor receptor–β (2.1) than malignant peripheral nerve sheath tumors (MPNSTs) (1.5, p = 0.004) and neurofibromas (1.33, p = 0.007). Expression of human epidermal growth factor receptor–2 was greater in SPSs (0.91) than in MPNSTs (0.33, p = 0.002) and neurofibromas (0.33, p = 0.026). Epidermal growth factor receptor was expressed in far fewer SPS cells (10%) than in MPNSTs (58%, p < 0.0001) or neurofibromas (37%, p = 0.007). SPSs more frequently expressed cytoplasmic survivin (66% of tumor cells) than normal nerve (46% of cells), but SPS expressed nuclear survivin in fewer tumor cells than in MPNSTs (24% and 50%, respectively; p = 0.018).CONCLUSIONSComplete resection is curative for SPS. Left untreated, however, these tumors can cause significant morbidity, and not all patients are candidates for resection. SPSs express a pattern of biomarkers consistent with the dysregulation of the tumor suppressor merlin observed in neurofibromatosis Type 2–associated schwannomas, suggesting a shared etiology. This SPS pattern is distinct from that of other tumors of the peripheral nerve sheath.


Biomaterials ◽  
2005 ◽  
Vol 26 (14) ◽  
pp. 2021-2031 ◽  
Author(s):  
Natalia Lago ◽  
Dolores Ceballos ◽  
Francisco J Rodrı́guez ◽  
Thomas Stieglitz ◽  
Xavier Navarro

Author(s):  
Alexander Scarborough ◽  
Robert J MacFarlane ◽  
Michail Klontzas ◽  
Rui Zhou ◽  
Mohammad Waseem

The upper limb consists of four major parts: a girdle formed by the clavicle and scapula, the arm, the forearm and the hand. Peripheral nerve lesions of the upper limb are divided into lesions of the brachial plexus or the nerves arising from it. Lesions of the nerves arising from the brachial plexus are further divided into upper (proximal) or lower (distal) lesions based on their location. Peripheral nerves in the forearm can be compressed in various locations and by a wide range of pathologies. A thorough understanding of the anatomy and clinical presentations of these compression neuropathies can lead to prompt diagnosis and management, preventing possible permanent damage. This article discusses the aetiology, anatomy, clinical presentation and surgical management of compressive neuropathies of the upper limb.


1990 ◽  
Vol 15 (1) ◽  
pp. 25-34
Author(s):  
D. MARSH

Erik Moberg pioneered the idea of validating measures of sensory function following peripheral nerve suture by correlating their results with those of functional tests. However it is important that powerful prior variables (age at suture, time elapsed since suture and delay between injury and suture) be controlled. Failure to do this may result in spurious correlations, as illustrated by analysis of two sets of data, one collected by the author and the other given in the classic paper of Önne (1962).


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